ArticleMolecular psychiatry2010
A SNAP25 promoter variant is associated with early-onset bipolar disorder and a high expression level in brain.
Article in Molecular psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 3 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 85 citations in OpenAlex.
- Biomarkers of Bipolar Disorder in Late Life: An Evidence-Based Systematic Review.Current psychiatry reports · 2024Pooled it
- Alterations in brain synaptic proteins and mRNAs in mood disorders: a systematic review and meta-analysis of postmortem brain studies.Molecular psychiatry · 2022Pooled it
- The genetics of early-onset bipolar disorder: A systematic review.Journal of affective disorders · 2015Pooled it
- Lithium-induced neuroprotection in bipolar disorder: Translational insights into cytoskeletal and proteomic mechanisms.IBRO neuroscience reports · 2025Review
- Molecular basis underlying changes of brain entropy and functional connectivity in major depressive disorders after electroconvulsive therapy.CNS neuroscience & therapeutics · 2024Article
- The Relationship between SNAP25 and Some Common Human Neurological Syndromes.Current pharmaceutical design · 2024Review
- Protein Misfolding and Aggregation in the Brain: Common Pathogenetic Pathways in Neurodegenerative and Mental Disorders.International journal of molecular sciences · 2022Review
- Syntaxin-1a and SNAP-25 expression level is increased in the blood samples of ischemic stroke patients.Scientific reports · 2022Article
- SNARER: new molecular descriptors for SNARE proteins classification.BMC bioinformatics · 2022Article
- CADPS functional mutations in patients with bipolar disorder increase the sensitivity to stress.Molecular psychiatry · 2022Article
- Dynamic Changes of Brain Cilia Transcriptomes across the Human Lifespan.International journal of molecular sciences · 2021Article
- Sarcopenia associates with SNAP-25 SNPs and a miRNAs profile which is modulated by structured rehabilitation treatment.Journal of translational medicine · 2021Article
- Contribution of common and rare damaging variants in familial forms of bipolar disorder and phenotypic outcome.Translational psychiatry · 2020Article
- Sex-Specific Proteomic Changes Induced by Genetic Deletion of Fibroblast Growth Factor 14 (FGF14), a Regulator of Neuronal Ion Channels.Proteomes · 2019Article
- Clinical correlates of age at onset distribution in bipolar disorder: a comparison between diagnostic subgroups.International journal of bipolar disorders · 2017Article
- A Multilevel Functional Study of aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- A genomic lifespan program that reorganises the young adult brain is targeted in schizophrenia.eLife · 2017Article
- Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats.Molecular neurobiology · 2017Article
- Genetic Studies on the Tripartite Glutamate Synapse in the Pathophysiology and Therapeutics of Mood Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Review
- Emerging Synaptic Molecules as Candidates in the Etiology of Neurological Disorders.Neural plasticity · 2017Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bipolar disorder (BD) is one of the most common and persistent psychiatric disorders. Early-onset BD has been shown to be the most severe and familial form. We recently carried out a whole-genome linkage analysis on sibpairs affected by early-onset BD and showed that the 20p12 region was more frequently shared in our families than expected by chance. The synaptosomal-associated protein SNAP25 is a presynaptic plasma membrane protein essential for the triggering of vesicular fusion and neurotransmitter release, and for which abnormal protein levels have been reported in postmortem studies of bipolar patients. We hypothesised that variations in the gene encoding SNAP25, located on chromosome 20p12, might influence the susceptibility to early-onset BD. We screened SNAP25 for mutations and performed a case-control association study in 197 patients with early-onset BD, 202 patients with late-onset BD and 136 unaffected subjects. In addition, we analysed the expression level of the two SNAP25 isoforms in 60 brains. We showed that one variant, located in the promoter region, was associated with early-onset BD but not with the late-onset subgroup. In addition, individuals homozygous for this variant showed a significant higher SNAP25b expression level in prefrontal cortex. These results show that variations in SNAP25, associated with an increased gene expression level in prefrontal cortex, might predispose to early-onset BD. Further analyses of this gene, as well as analysis of genes encoding for the SNAP25 protein partners, are required to understand the impact of such molecular mechanisms in BD.
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